Immunoinflammatory Biomarkers in Serum Are Associated with Disease Severity in Atopic Dermatitis

Dermatology ◽  
2021 ◽  
pp. 1-8
Author(s):  
Jesper Grønlund Holm ◽  
Guillem Hurault ◽  
Tove Agner ◽  
Maja Lisa Clausen ◽  
Sanja Kezic ◽  
...  

Background: A growing body of evidence links various biomarkers to atopic dermatitis (AD). Still, little is known about the association of specific biomarkers to disease characteristics and severity in AD. Objective: To explore the relationship between various immunological markers in the serum and disease severity in a hospital cohort of AD patients. Methods: Outpatients with AD referred to the Department of Dermatology, Bispebjerg Hospital, Copenhagen, Denmark, were divided into groups based on disease severity (SCORAD). Serum levels of a preselected panel of immunoinflammatory biomarkers were tested for association with disease characteristics. Two machine learning models were developed to predict SCORAD from the measured biomarkers. Results: A total of 160 patients with AD were included; 53 (33.1%) with mild, 73 (45.6%) with moderate, and 34 (21.3%) with severe disease. Mean age was 29.2 years (range 6–70 years) and 84 (52.5%) were females. Numerous biomarkers showed a statistically significant correlation with SCORAD, with the strongest correlations seen for CCL17/thymus and activation-regulated chemokine (chemokine ligand-17/TARC) and CCL27/cutaneous T cell-attracting-chemokine (CTACK; Spearman R of 0.50 and 0.43, respectively, p < 0.001). Extrinsic AD patients were more likely to have higher mean SCORAD (p < 0.001), CCL17 (p < 0.001), CCL26/eotaxin-3 (p < 0.001), and eosinophil count (p < 0.001) than intrinsic AD patients. Predictive models for SCORAD identified CCL17, CCL27, serum total IgE, IL-33, and IL-5 as the most important predictors for SCORAD, but with weaker associations than single cytokines. Conclusions: Specific immunoinflammatory biomarkers in the serum, mainly of the Th2 pathway, are correlated with disease severity in patients with AD. Predictive models identified biomarkers associated with disease severity but this finding warrants further investigation.

2006 ◽  
Vol 2006 ◽  
pp. 1-4 ◽  
Author(s):  
Murat Aral ◽  
Ozer Arican ◽  
Mustafa Gul ◽  
Sezai Sasmaz ◽  
Sumeyra Alkis Kocturk ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Henrique Pott-Junior ◽  
Natália Queiroz Prado Bittencourt ◽  
Silvana F. G. Chacha ◽  
Rafael Luís Luporini ◽  
Marcia Regina Cominetti ◽  
...  

Liver involvement in COVID-19 is not yet well-understood, but elevations in liver transaminases have been described to occur in 14–53% of the cases and are more frequently seen in severe disease. This cross-sectional study explored the relationship between the elevations in liver transaminases and inflammatory parameters in 209 adults with COVID-19. Demographic and clinical data, serum levels of inflammatory cytokines and liver aminotransferases were analyzed. Three groups were formed according to the liver transaminase abnormalities: (I) Normal transaminases, (II) Borderline transaminases elevation, and (III) Mild to severe transaminases elevation. Altered liver transaminases were directly related to disease severity, showing association with the NEWS2 score at admission and greater need for ICU or death. Moreover, higher levels of IL-2 and CRP were associated with borderline transaminases elevations, whereas higher levels of IL-10 and Neutrophil to Lymphocyte ratio were associated with mild to severe transaminases elevation. These results reinforce the importance of liver transaminases in patients with COVID-19 as a complementary marker for disease severity and also point to them as a parameter reflecting the continuous dynamics between viral infection and the immune response.


2020 ◽  
Vol 2020 ◽  
pp. 1-7 ◽  
Author(s):  
Pavel Borsky ◽  
Zdenek Fiala ◽  
Ctirad Andrys ◽  
Martin Beranek ◽  
Kvetoslava Hamakova ◽  
...  

Background. Psoriasis vulgaris is a chronic autoimmune disease associated with systemic inflammation. Increased levels of numerous cytokines, chemokines, growth factors, and other molecules were found in the skin and in the circulation of psoriatic patients. Alarmins, also known as danger signals, are intracellular proteins, which are released to an extracellular space after infection or damage. They are the markers of cell destructive processes. Objective. The aim of the present study was to evaluate the suitability of selected alarmins (HMGB1, IL-33, S100A7, and S100A12) as potential biomarkers of severity of psoriasis and to explore possible relationships between these proteins for the purpose of better understanding their roles in the immunopathology of psoriasis. Methods. The serum levels of selected alarmins were measured in 63 psoriatic patients and 95 control individuals. The levels were assessed by the ELISA technique using commercial kits. The data were statistically processed with MedCalc version 19.0.5. Results. In psoriatic patients, we found significantly increased levels of HMGB1 (p<0.05), IL-33 (p<0.01), S100A7 (p<0.0001), and S100A12 (p<0.0001). In addition, we found a significant relationship between HMGB1 and S100A7 (Spearman’s rho=0.276, p<0.05) in the patients and significant relationship between HMGB1 and IL-33 in the controls (Spearman’s rho=0.416, p<0.05). We did not find any relationship between observed alarmins and the disease severity. Conclusions. The alarmins HMGB1, IL-33, S100A7, and S100A12 were significantly elevated in the serum of patients, which states the hypothesis that they play specific roles in the immunopathology of psoriasis. However, we have not yet found a relationship between observed alarmins and the disease severity. The discovery of the relationship between HMGB1 and S100A7 is a novelty that should be studied in the future to further clarify its role and importance.


2011 ◽  
Vol 36 (7) ◽  
pp. 728-732 ◽  
Author(s):  
M. Trzeciak ◽  
J. Gleń ◽  
T. Bandurski ◽  
M. Sokołowska-Wojdyło ◽  
A. Wilkowska ◽  
...  

2021 ◽  
pp. 026835552110233
Author(s):  
Mikel Sadek ◽  
Matthew Pergamo ◽  
Jose I Almeida ◽  
Glenn R Jacobowitz ◽  
Lowell S Kabnick

Objectives The purpose was to assess whether combining patient reported scores (VVSymQ®) and physician reported scores (VCSS) stratifies disease severity in C2 patients. Methods Consecutive patients were pooled from the VANISH-1 and VANISH-2 cohorts. VCSS and VVSymQ® were calculated for each patient. The relationship between scoring systems was evaluated using Pearson’s correlation and frequency distribution analysis. Results Two-hundred and ten C2 limbs were included. Scoring systems demonstrated: VVSymQ®: mean = 8.72; VCSS: mean = 6.32; correlation (r = 0.22, p = 0.05). Frequency distribution analysis demonstrated 61.4% of patients had low VVSymQ® and low VCSS; 31.3% had elevated VVSymQ® and increased VCSS; 7.3% were inconsistent with C2 disease. Strict concordance analysis revealed 40.5% had VVSymQ® (< 9)/VCSS (0-6), 18.6% had VVSymQ® (≥ 9)/VCSS (7-9), and 2.9% had VVSymQ® (≥9)/VCSS (≥10). Conclusions For combined elevated VVSymQ® and VCSS, moderate/severe disease is corroborated, and intervention may be indicated. For combined lower scores, the disease severity is mild and conservative therapy is more appropriate.


2021 ◽  
Author(s):  
Montse Marquès ◽  
Eudald Correig ◽  
Daiana Ibarretxe ◽  
Eva Anoro ◽  
Juan Antonio Arroyo ◽  
...  

Abstract A retrospective observational study with patients suffering COVID-19 was performed to assess the underlying effect of long-term exposure to NO2 and PM10 on the COVID-19 outcomes. We built multivariate predictive models to assess the relationship between the long-term exposure to NO2 and PM10 and COVID-19 outcomes. The probability of either death or severe COVID-19 outcome and the percentage of dead or severe patients were predicted, while odds ratios and effects estimates were calculated. Whilst the long-term exposure to NO2 is a variable with a rather low importance in the prediction of COVID-19 health outcomes, the long-term exposure to PM10 is a more important variable than some stated comorbidities. PM10 showed the highest effects estimates (1.65, 95% CI 1.32-2.06) on COVID-19 severity. For mortality, the highest effect estimates corresponded to age (3.59, 95% CI 2.94-4.40), followed by PM10 (2.37, 95% CI 1.71-3.32). Finally, an increase of 1 µg/m3 in PM10 concentration causes an increase of 3.06% (95% CI 1.11%-4.25%) and 2.68% (95% CI 0.53%-5.58%) of patients suffering COVID-19 as a severe disease and deaths, respectively. These results demonstrate that long-term PM10 burdens above WHO guidelines exacerbate COVID-19 outcomes, while it must be considered for an accurate medical prognosis of COVID-19.


Author(s):  
Duco Koenis ◽  
Issa Beegun ◽  
Charlotte Jouvene ◽  
Gabriel Amador Aguirre ◽  
Patricia R Souza ◽  
...  

Rationale: Resolution mechanisms are central in both the maintenance of homeostasis and the return to catabasis following tissue injury and/or infections. Amongst the pro-resolving mediators, the essential fatty acid-derived specialized pro-resolving lipid mediators (SPM) govern immune responses to limit disease severity. Notably, little is known about the relationship between the expression and activity of SPM pathways, circulating phagocyte function and disease severity in patients infected with novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) leading to coronavirus disease 2019 (COVID-19). Objective: Herein, we investigated the link between circulating SPM concentrations and phagocyte activation status and function in COVID-19 patients (n=39) compared to healthy (n=12) and post-COVID-19 (n=8) volunteers. Methods and Results: Lipid mediator profiling demonstrated that plasma SPM concentrations were upregulated in patients with mild COVID-19 and are downregulated in those with severe disease. SPM concentrations were correlated with both circulating phagocyte activation status and function. Perturbations in plasma SPM concentrations and phagocyte activation were retained after the resolution of COVID-19 clinical symptoms. Treatment of patients with dexamethasone upregulated both the expression of SPM biosynthetic enzymes in circulating phagocytes and plasma concentration of these mediators. Furthermore, incubation of phagocytes from COVID-19 patients with SPM rectified their phenotype and function. This included a downregulation in the expression of activation markers, a decrease in the Tissue Factor and inflammatory cytokine expression, and an upregulation of bacterial phagocytosis. Conclusions: The present findings suggest that downregulation of systemic SPM concentrations is linked with both increased disease severity and dysregulated phagocyte function. They also identify the upregulation of these mediators by dexamethasone as a potential mechanism in host protective activities elicited by this drug in COVID-19 patients. Taken together, our findings elucidate a role for altered resolution mechanisms in the disruption of phagocyte responses and the propagation of systemic inflammation in COVID-19.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A278-A278
Author(s):  
Luigi di Filippo ◽  
Agnese Allora ◽  
Mauro Doga ◽  
Patrizia Rovere Querini ◽  
Massimo Locatelli ◽  
...  

Abstract High prevalence of vitamin D (VD) deficiency in COVID-19 patients was reported by several studies. Since VD is a key regulating factor of both innate and adaptive immunity, it was hypothesized that VD deficiency may predispose to SARS-CoV-2 infection and lower levels of VD could be related to increased COVID-19 severity and worse outcome risks. However, to date, only few studies partially investigated the relationship between VD and inflammatory and immune response and clinical features of COVID-19 patients. The aim of this study is to evaluate the influence of vitamin D levels on COVID-19 inflammatory activity, clinical pattern and disease severity. Patients admitted to San Raffaele University Hospital for COVID-19 from February 2020 were enrolled in this study. We excluded patients with comorbidities and therapies influencing VD metabolism. 25OH-Vitamin D levels were evaluated at admission in hospital and VD insufficiency and deficiency were defined as VD level below 30 ng/mL and 20 ng/mL, respectively. A total of 88 patients were included in the study. Median (IQR) VD levels were 16.3 (11.2–23.9) ng/mL. VD insufficiency and deficiency were found in 88.6% and in 68.2% of patients, respectively. Linear regression analyses showed a positive correlation between VD levels and PaO2/FiO2 ratio (p=0.019; r=0.254), and negative correlations between VD levels and Neutrophil/Lymphocyte (N/L) ratio (p=0.04; r=-0.19), C-reactive protein (CRP) levels (p=0.047; r=-0.18) and Interleukin 6 (IL-6) levels (p=0.04; r=-0.22). Lower VD levels were found in patients affected by severe disease (needs for high-flow oxygen therapy and/or noninvasive mechanical ventilation, admitted to ICU and/or dead) than non-severe patients (13.4 ng/mL [10.37–19.15] vs 18.45 ng/mL [15.15–24.95]; p=0.007). Moreover, patients with VD deficiency had higher levels of CRP, LDH, IL-6, IFN-gamma (p=0.04, p=0.01, p=0.002, p=0.04; respectively), lower PaO2/FiO2 and higher N/L ratios (p=0.008, p=0.004; respectively), and higher rate of severe disease (65% vs 39%, p=0.02), as compared to VD non-deficient ones. In conclusion, low VD levels are widely found in hospitalized COVID-19 and may lead to increased disease severity through an excessive immune-inflammatory response. Our data suggest that reaching adequate vitamin D levels in risky population may contribute to prevention of COVID-19 occurrence and severity.


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